HCMC_P_049062 - Hennepin County Medical Center

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Case Reports Figure Two. The cardiac monitor strip showing a wide complex tachycardia, likely AIVR Figure Three. The Inspiratory Threshold Device Figure Four. The ResQPump ® and stents were placed at each lesion. Following PCI, an intra-aortic balloon pump was placed due to cardiogenic shock with elevated left ventricular enddiastolic pressure and resulting pulmonary edema. (This has since been shown to be ineffective in cardiogenic shock in STEMI.) 1 The patient developed an intermittent wide complex rhythm which at first was interpreted as ventricular tachycardia (VT) (Figure Two). He was started briefly on amiodarone and it was subsequently stopped when the rhythm was reassessed. The diagnosis of VT was not certain because of a relatively slow heart rate. Instead, an accelerated idioventricular rhythm (AIVR) was considered. AIVR is differentiated from ventricular tachycardia by the heart rate: AIVR is < 120 bpm, while ventricular tachycardia is almost always > 120 bpm. AIVR is a common reperfusion dysrhythmia and is good evidence of reperfusion of STEMI (in other words, a good sign). It does not require any treatment unless associated with hypotension. By 24 hours, the balloon pump could be removed. Serial troponin I peaked at 13.7 ng/ml, which is far lower than expected for a STEMI of this size and suggests that total occlusion time was brief. Initial transthoracic echocardiogram on day 2 showed an ejection fraction (EF) of 15-20% (normal, 65-70%); with septal and apical wall motion abnormalities (WMA). Thus, as is usual, the myocardium was “stunned,” though not all infarcted. The EF greatly improved by 2 days later, when a repeated echocardiogram revealed an EF 35% and corresponding improvement in WMA. At 48 hours, the patient had completed the hypothermia protocol without complication and was extubated, at which time he was following simple commands but had anterograde amnesia. By 72 hours, his neurological status had greatly improved; anterograde amnesia was resolving but there was no memory of events. He recovered fully and was discharged on prasugrel, aspirin, lisinopril, carvedilol, atorvastatin, and eplerenone. After cardiac rehabilitation, his ejection fraction returned to normal and he was again able to bike 50 miles at a time. He has had no further symptoms. Discussion More information on Compression Decompression CPR, the Inspiratory Threshold Device, and the LUCAS device is available at http://www.naph.org/ Homepage-Sections/Explore/Innovations/Heart- Health/Hennepin-County-Medical-Center.aspx. In January 2011, investigators, including several from HCMC, published the results of a randomized trial comparing compression-decompression CPR to standard CPR in out-of-hospital cardiac arrest, and found that 74 (9%) of 840 patients survived to 1 year in the intervention group compared with 48 (6%) of 813 controls (p=0·03), with equivalent cognitive skills, disability ratings, and emotional-psychological status in both groups. 2 In the compression-decompression group, first responders used both the ITD (ResQPod ® ), (Figure Three) and a specially designed compressiondecompression device called the ResQPump ® (Figure Four). The ResQPump ® has a suction cup that attaches to the chest, and when pulled up forcefully, may create 30 pounds of negative pressure in the chest, augmenting the pumping action of the chest. The ITD is placed on the endotracheal tube and has a valve that stays closed for a fraction of a second, preventing that negative pressure from drawing air down the endotracheal tube, ensuring that there will be negative pressure to draw blood into the chest and into the heart, for further pumping out to the body with each compression. The two together, then, increased survival with good neurologic outcome (Modified Rankin Score of 3 or less) by 50%. The LUCAS device (Figure Five) combines mechanical compression that is uniform and does not fatigue with suction for decompression, but with less suction. It provides 2 inches of chest compression at 4 | Approaches in Critical Care | January 2013
Case Reports Figure Five. The LUCAS device several pounds of negative force. Newer software automatically adjusts the plunger to ensure good contact with the sternum. It is unlike human CPR, which degrades due to fatigue or distraction, and is often done at a rate too slow or too fast for optimal blood flow, does not allow for full chest wall recoil as the provider tends to lean on the chest, and must be stopped during administration of shocks. It has been shown to improve blood flow in experimental models and anecdotal reports in humans. We have found in some cases that it creates exceptional blood pressure in ED cardiac arrest patients, as measured by arterial line; and it is more likely than manual chest compression to keep the brain perfused (and therefore alive) in prolonged arrest. The LUCAS device also allows safe transport of the patient with ongoing CPR, thus making it possible to go to the cath lab with ongoing CPR. Therapeutic Hypothermia In 2002, 2 randomized studies in the New England Journal of Medicine compared therapeutic cooling for 24 hours to standard care. 3, 4 These trials, and evidence from dog studies, form the basis of this now standard therapy for comatose survivors of cardiac arrest. In these studies, patients who were resuscitated from pulseless ventricular fibrillation (VF) or tachycardia (VT) were randomized within 3 hours, and those who underwent hypothermia were sedated, chemically paralyzed, and externally cooled to a target temperature of 32 to 34 degrees Celsius, where they were kept for 24 hours before rewarming. Only 8% of cardiac arrest patients met eligibility criteria. The primary endpoint was good neurologic outcome at 6 months, which, when combining the 2 studies, was achieved in the hypothermia group in 54% vs. 37%. Mortality was 43% vs. 58%. Adverse events were not different between the groups. Based on this, the International Liaison Committee on Resuscitation advised use of therapeutic hypothermia, to 32-34 degrees for 12 to 24 hours, for unconscious adult patients with return of spontaneous circulation after out-of-hospital ventricular fibrillation arrest. 5 Therapeutic hypothermia requires intubation and paralysis and very intensive monitoring for electrolyte shifts and dysrhythmias. Conclusion Since 2003, we at Hennepin County Medical Center have cooled comatose survivors of cardiac arrest. We have decided to broaden the indications for the therapy beyond those with VF or VT to those patients who have been resuscitated from asystole, pulseless electrical activity (PEA) and respiratory etiologies of cardiac arrest, as long as they have return of spontaneous circulation within 60 minutes of arrest. From January 2008 through December 2011, Hennepin had 129 patients resuscitated after cardiac arrests who were eligible for and underwent therapeutic hypothermia: 86 had VF or VT, and 43 had PEA or asystole. Of the 129, 61 (47%) survived with good neurologic outcome; 6 of these had PEA or asystole as the initial rhythm. In total, 57 (44%) died, 35 of whom had asystole or PEA. There were 11 survivors, but with poor neurologic outcomes; 2 of these had asystole or PEA. The 56 of 86 (65%) with a shockable rhythm survived with good neurologic outcome. Most of these were before the use of the LUCAS device. This case and our survival statistics illustrate the rapid advancements occurring in the management of patients with cardiac arrest. Combining new therapies, such as those described in this case report, has the potential to improve survival even more. References 1. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med 2012; 367(14):1287-96. 2. Aufderheide TP, Frascone RJ, Wayne MA, et al. Standard cardiopulmonary resuscitation versus active compressiondecompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: a randomised trial. Lancet 2011;377(9762):301-11. 3. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002; 346(8):557-63. 4. The_Hypothermia_after_Cardiac_Arrest_Study_Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346(8):549-56. 5. Nolan JP, Morley PT, Hoek TL, Hickey RW. Therapeutic hypothermia after cardiac arrest. An advisory statement by the Advancement Life support Task Force of the International Liaison committee on Resuscitation. Resuscitation 2003;57(3):231-5. Approaches in Critical Care | January 2013 | 5
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